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Related Concept Videos

Amyloid Fibrils03:03

Amyloid Fibrils

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Amyloid fibrils are aggregates of misfolded proteins.  Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils. 
Amyloid deposits were observed as early as 1639 in the liver and the spleen.   In 1854, Rudolph Virchow performed iodine staining,...
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Related Experiment Video

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Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease
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Genetically identical twin-pair difference models support the amyloid cascade hypothesis.

Emma M Coomans1,2, Jori Tomassen3,4, Rik Ossenkoppele3,4,5

  • 1Department of Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam, Amsterdam UMC location VUmc, 1081 HV Amsterdam, The Netherlands.

Brain : a Journal of Neurology
|March 9, 2023
PubMed
Summary
This summary is machine-generated.

This study in identical twins shows amyloid-beta

Keywords:
Alzheimer’s diseaseamyloid-βcognitionidentical twinsneurodegenerationtau

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Area of Science:

  • Neuroscience
  • Genetics
  • Alzheimer's Disease Research

Background:

  • The amyloid cascade hypothesis is central to Alzheimer's disease (AD) research, yet the precise mechanism linking amyloid-beta (Aβ) pathology to tau aggregation remains unclear.
  • Alternative hypotheses suggest shared upstream processes may drive both Aβ and tau independently, rather than a direct causal link.
  • Investigating these relationships within genetically identical twins can control for genetic and shared environmental confounders.

Purpose of the Study:

  • To test the causal relationship between amyloid-beta (Aβ) and tau pathology in Alzheimer's disease using genetically identical twin-pair difference models.
  • To assess the association between Aβ, tau, neurodegeneration, and cognitive decline, controlling for genetic and environmental factors.
  • To determine the mediating role of tau and neurodegeneration in the effects of Aβ on cognitive decline.

Main Methods:

  • Utilized positron emission tomography (PET) imaging for longitudinal Aβ ([18F]flutemetamol) and cross-sectional tau ([18F]flortaucipir) in 78 cognitively unimpaired identical twins.
  • Assessed neurodegeneration via MRI (hippocampal volume) and cognitive function (composite memory).
  • Employed generalized estimating equation models at the individual level and within-pair difference models to analyze associations and mediation, controlling for genetic and shared environmental influences.

Main Results:

  • Strong associations were observed between Aβ, tau, neurodegeneration, and cognition at the individual level.
  • Within-pair difference analyses confirmed these associations, with significant links between Aβ and tau (β = 0.68), Aβ and hippocampal volume (β = -0.37), and Aβ and memory (β = -0.57).
  • Tau pathology significantly mediated the effects of Aβ on neurodegeneration and cognitive decline, with 51.6% of the Aβ effect on memory mediated through tau.

Conclusions:

  • Associations between Aβ, tau, neurodegeneration, and cognition in identical twins are robust and not confounded by genetic or shared environmental factors.
  • The findings strongly support the amyloid cascade hypothesis, demonstrating that tau pathology mediates the neurodegenerative and cognitive effects of Aβ.
  • These results provide critical evidence for refining Alzheimer's disease research and clinical trial designs, emphasizing the role of tau in the disease pathway.